Control of melanoma cell invasion by type IV collagen

2005 ◽  
Vol 29 (3) ◽  
pp. 260-266 ◽  
Author(s):  
Sylvie Pasco ◽  
Bertrand Brassart ◽  
Laurent Ramont ◽  
François-Xavier Maquart ◽  
Jean-Claude Monboisse
1990 ◽  
Vol 111 (1) ◽  
pp. 261-270 ◽  
Author(s):  
M K Chelberg ◽  
J B McCarthy ◽  
A P Skubitz ◽  
L T Furcht ◽  
E C Tsilibary

The adhesion and motility of tumor cells on basement membranes is a central consideration in tumor cell invasion and metastasis. Basement membrane type IV collagen directly promotes the adhesion and migration of various tumor cell types in vitro. Our previous studies demonstrated that tumor cells adhered and spread on surfaces coated with intact type IV collagen or either of the two major enzymatically purified domains of this protein. Only one of these major domains, the pepsin-generated major triple helical fragment, also supported tumor cell motility in vitro, implicating the involvement of the major triple helical region in type IV collagen-mediated tumor cell invasion in vivo. The present studies extend our previous observations using a synthetic peptide approach. A peptide, designated IV-H1, was derived from a continuous collagenous region of the major triple helical domain of the human alpha 1(IV) chain. This peptide, which has the sequence GVKGDKGNPGWPGAP, directly supported the adhesion, spreading, and motility of the highly metastatic K1735 M4 murine melanoma cell line, as well as the adhesion and spreading of other cell types, in a concentration-dependent manner in vitro. Furthermore, excess soluble peptide IV-H1, or polyclonal antibodies directed against peptide IV-H1, inhibited type IV collagen-mediated melanoma cell adhesion, spreading, and motility, but had no effect on these cellular responses to type I collagen. The full complement of cell adhesion, spreading, and motility promoting activities was dependent upon the preservation of the three prolyl residues in the peptide IV-H1 sequence. These studies indicate that peptide IV-H1 represents a cell-specific adhesion, spreading, and motility promoting domain that is active within the type IV collagen molecule.


1996 ◽  
Vol 7 (3) ◽  
pp. 383-396 ◽  
Author(s):  
J R Knutson ◽  
J Iida ◽  
G B Fields ◽  
J B McCarthy

Tumor cell invasion of basement membranes (BM) represents one of the critical steps in the metastatic process. Tumor cell recognition of individual BM matrix components may involve individual cell adhesion receptors, such as integrins or cell surface proteoglycans, or may involve a coordinate action of both types of receptors. In this study, we have focused on the identification of a cell surface CD44/chondroitin sulfate proteoglycan (CSPG) and alpha 2 beta 1 integrin on human melanoma cells that are both directly involved in the in vitro invasion of reconstituted BM via a type IV collagen-dependent mechanism. Interfering with cell surface expression of human melanoma CSPG with either p-nitro-phenyl-beta-D-xylopyranoside treatment or anti-CD44 monoclonal antibody (mAb) preincubation (mAb) preincubation inhibits melanoma cell invasion through reconstituted BM. These treatments also strongly inhibit melanoma cell migration on type IV collagen, however, they are ineffective at inhibiting cell adhesion to type IV collagen. Purified melanoma cell surface CD44/CSPG, or purified chondroitin sulfate, bind to type IV collagen affinity columns, consistent with a role for CD44/CSPG-type IV collagen interactions in mediating tumor cell invasion. In contrast, melanoma cell migration on laminin (LM) does not involve CD44/CSPG, nor does CD44/CSPG bind to LM, suggesting that CD44/CSPG-type IV collagen interactions are specific in nature. Additionally, anti-alpha 2 and anti-beta 1 integrin mAbs are capable of blocking melanoma cell invasion of reconstituted BM. Both of these anti-integrin mAbs inhibit melanoma cell adhesion and migration on type IV collagen, whereas only anti-beta 1 mAb inhibits cell adhesion to LM. Collectively, these results indicate that melanoma cell adhesion to type IV collagen is an important consideration in invasion of reconstituted BM in vitro, and suggest that CD44/CSPG and alpha 2 beta 1 integrin may collaborate to promote human melanoma cell adhesion, migration, and invasion in vivo.


2004 ◽  
Vol 279 (42) ◽  
pp. 43503-43513 ◽  
Author(s):  
Diane Baronas-Lowell ◽  
Janelle L. Lauer-Fields ◽  
Jeffrey A. Borgia ◽  
Gian Franco Sferrazza ◽  
Mohammad Al-Ghoul ◽  
...  

PLoS Genetics ◽  
2016 ◽  
Vol 12 (2) ◽  
pp. e1005905 ◽  
Author(s):  
Meghan A. Morrissey ◽  
Ranjay Jayadev ◽  
Ginger R. Miley ◽  
Catherine A. Blebea ◽  
Qiuyi Chi ◽  
...  

2014 ◽  
Vol 289 (31) ◽  
pp. 21591-21604 ◽  
Author(s):  
Maciej J. Stawikowski ◽  
Beatrix Aukszi ◽  
Roma Stawikowska ◽  
Mare Cudic ◽  
Gregg B. Fields

Oncogene ◽  
2003 ◽  
Vol 22 (1) ◽  
pp. 98-108 ◽  
Author(s):  
Louis Hodgson ◽  
Andrew J Henderson ◽  
Cheng Dong

1997 ◽  
Vol 40 (19) ◽  
pp. 3077-3084 ◽  
Author(s):  
Janelle L. Lauer ◽  
Leo T. Furcht ◽  
Gregg B. Fields

1989 ◽  
Vol 93 (1) ◽  
pp. 155-161
Author(s):  
M. Edward ◽  
J.A. Gold ◽  
R.M. MacKie

The effect of retinoic acid pretreatment on metastatic B16 melanoma cell adhesion in serum-free medium to tissue culture plastic precoated with fibronectin, laminin/nidogen, type I and type IV collagen was examined. Both control cells grown to subconfluence and cells treated with 10(−6) M-retinoic acid adhered and spread rapidly on fibronectin (greater than 75% following 1 h of incubation) but adhered poorly to type I collagen (less than 15%). Control cells adhered to laminin/nidogen (greater than 35%), type IV collagen (greater than 58%) and type IV collagen plus laminin/nidogen (greater than 80%), while retinoic acid-treated cells showed a reduced ability to attach and spread on these substrata, the number of adherent cells being reduced by 61% on laminin/nidogen, by 19% on type IV collagen, and by 41% on type IV collagen plus laminin/nidogen following 1 h of incubation. The minimum concentration of retinoic acid required to yield an effective reduction in adhesion was 10(−7) M for type IV collagen and 10(−10) M for laminin/nidogen. Melanoma cells harvested at low density showed a reduced adhesion to laminin/nidogen and type IV collagen compared to that of subconfluent control cultures, but also showed a reduced adhesion to fibronectin. The effect of retinoic acid on cell adhesion was not, however, due to reduced cell density, as the cells were seeded so that control and retinoic acid-treated cultures were of a similar density when harvested.


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